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. 2012 May 23;32(21):7278–7286. doi: 10.1523/JNEUROSCI.6273-11.2012

Figure 4.

Figure 4.

PKCε mediates Lck activation in PC. A, B, Pretreatment with εV1-2 (PCKε inhibitor; 10 μm) using BioPORTER abolished NMDA PC neuroprotection in PI-staining (A) or LDH leakage (B). Pharmacological activation of PKCε by ψεRACK (10 μm) demonstrated a similar effect as NMDA PC. *p < 0.05, **p < 0.01 versus NMDA lethal; #p < 0.05 versus NMDA PC+NMDA lethal. C, Colocalization of PKCε with Lck was increased by NMDA PC. Lck or PKCε in each Lck-immunoprecipitates were examined by Western blot. D, Inhibition of PKCε by εV1-2 reversed NMDA PC-induced Lck kinase activation. εV1-2 (10 μm) was treated by BioPORTER before PC, and cell lysates were collected for Lck immunoprecipitation and kinase assay. *p < 0.05 versus control without PC; #p < 0.05 versus NMDA PC. A–D, n = 3. All values are means ± SEM and analyzed by Student's t test.